Mei Sun1, Guolei Tan1, Jinyun Song1, Jianfang Wang1, Xuping Wu2. 1. The Second Hospital of Nanjing affiliated to Medical School of Southeast University, 210003 Nanjing, China. 2. The Second Hospital of Nanjing affiliated to Medical School of Southeast University, 210003 Nanjing, China. Electronic address: xuping_wu@yahoo.com.
Abstract
BACKGROUND/AIMS: We investigated the efficacy of entecavir (ETV) monotherapy in 54 naïve patients and 27 lamivudine (LMV) and/or adefovir (ADV) experienced patients. METHODS: Eighty-one chronic hepatitis B patients with a viral load above 4 log 10 copies/ml and high levels of serum alanine aminotransferase were treated with ETV 0.5mg daily. The viruses of patients were sequenced before ETV therapy and after every three months of ETV therapy. RESULTS: Eight LAM-experienced and ADV-experienced patients emerged mutations in the ETV treatment. In one of these experienced patients, the ETV-resistant mutations were detected during ETV treatment, with the virological and the biochemical breakthrough. Two LAM-experienced and ADV-naïve patients were detected mutation during 1-2 years ETV therapy. All three LAM-naïve and ADV-experienced patients were detected mutations in the ETV treatment. Five in fifty for LAM-naïve and ADV-naïve patients showed mutations in the ETV monotherapy. CONCLUSIONS: ETV has a high genetic barrier to resistance and the efficacy in LAM-experienced and/or ADV-experienced patients were much lower than in naïve patients.
BACKGROUND/AIMS: We investigated the efficacy of entecavir (ETV) monotherapy in 54 naïve patients and 27 lamivudine (LMV) and/or adefovir (ADV) experienced patients. METHODS: Eighty-one chronic hepatitis Bpatients with a viral load above 4 log 10 copies/ml and high levels of serum alanine aminotransferase were treated with ETV 0.5mg daily. The viruses of patients were sequenced before ETV therapy and after every three months of ETV therapy. RESULTS: Eight LAM-experienced and ADV-experienced patients emerged mutations in the ETV treatment. In one of these experienced patients, the ETV-resistant mutations were detected during ETV treatment, with the virological and the biochemical breakthrough. Two LAM-experienced and ADV-naïve patients were detected mutation during 1-2 years ETV therapy. All three LAM-naïve and ADV-experienced patients were detected mutations in the ETV treatment. Five in fifty for LAM-naïve and ADV-naïve patients showed mutations in the ETV monotherapy. CONCLUSIONS:ETV has a high genetic barrier to resistance and the efficacy in LAM-experienced and/or ADV-experienced patients were much lower than in naïve patients.